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N’-(2-hydroxybenzoyl)nicotinohydrazide is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

300799-72-8

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300799-72-8 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 300799-72-8 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 3,0,0,7,9 and 9 respectively; the second part has 2 digits, 7 and 2 respectively.
Calculate Digit Verification of CAS Registry Number 300799-72:
(8*3)+(7*0)+(6*0)+(5*7)+(4*9)+(3*9)+(2*7)+(1*2)=138
138 % 10 = 8
So 300799-72-8 is a valid CAS Registry Number.

300799-72-8Downstream Products

300799-72-8Relevant academic research and scientific papers

Complexes of unsymmetric bis-hydrazide ligands: Crystal structures and properties

Zhou, Ying-Xia,Yuan, Rui-Fang,Fan, Cai-Ling,Liu, Li-E,Wu, Ben-Lai,Zhang, Hong-Yun

, p. 3133 - 3146 (2012)

Two unsymmetric bis-aroyl-hydrazines, N-(2-hydroxybenzoyl) isonicotinohydrazide (L1) and N-(2-hydroxybenzoyl)nicotinohydrazide (L2), were synthesized through reactions of salicyl hydrazide with isonicotinoyl chloride and nicotinoyl chloride, respectively.

METHOD OF MODULATING RIBONUCLEOTIDE REDUCTASE

-

, (2020/02/14)

A method of modulating ribonucleotide reductase activity in a neoplastic cell includes administering to the cell an amount of a hydrazone or hydrazine ribonucleotide reductase modulator (RRmod), the amount being effective to inhibit neoplastic cell growth.

Structure-guided design of anti-cancer ribonucleotide reductase inhibitors

Misko, Tessianna A.,Liu, Yi-Ting,Harris, Michael E.,Oleinick, Nancy L.,Pink, John,Lee, Hsueh-Yun,Dealwis, Chris G.

, p. 438 - 450 (2019/01/14)

Ribonucleotide reductase (RR) catalyses the rate-limiting step of dNTP synthesis, establishing it as an important cancer target. While RR is traditionally inhibited by nucleoside-based antimetabolites, we recently discovered a naphthyl salicyl acyl hydrazone-based inhibitor (NSAH) that binds reversibly to the catalytic site (C-site). Here we report the synthesis and in vitro evaluation of 13 distinct compounds (TP1-13) with improved binding to hRR over NSAH (TP8), with lower KD’s and more predicted residue interactions. Moreover, TP6 displayed the greatest growth inhibiting effect in the Panc1 pancreatic cancer cell line with an IC50 of 0.393 μM. This represents more than a 2-fold improvement over NSAH, making TP6 the most potent compound against pancreatic cancer emerging from the hydrazone inhibitors. NSAH was optimised by the addition of cyclic and polar groups replacing the naphthyl moiety, which occupies the phosphate-binding pocket in the C-site, establishing a new direction in inhibitor design.

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